{Reference Type}: Journal Article
{Title}: Emodin alleviates intestinal ischemia-reperfusion injury through antioxidant stress, anti-inflammatory responses and anti-apoptosis effects via Akt-mediated HO-1 upregulation.
{Author}: Liu Y;Ji T;Jiang H;Chen M;Liu W;Zhang Z;He X;
{Journal}: J Inflamm (Lond)
{Volume}: 21
{Issue}: 1
{Year}: 2024 Jul 9
{Factor}: 6.283
{DOI}: 10.1186/s12950-024-00392-z
{Abstract}: <B>BACKGROUND: </B>Intestinal ischemia-reperfusion (I/R) injury is a severe vascular emergency. Previous research indicated the protective effects of Emodin on I/R injury. Our study aims to explore the effect of Emodin on intestinal I/R (II/R) injury and elucidate the underlying mechanisms.<BR><B>METHODS: </B>C57BL/6 mice and Caco-2 cells were used for in vivo and in vitro studies. We established an animal model of II/R injury by temporarily occluding superior mesenteric artery. We constructed an oxygen-glucose deprivation/reoxygenation (OGD/R) cell model using a hypoxia-reoxygenation incubator. Different doses of Emodin were explored to determine the optimal therapeutic dose. Additionally, inhibitors targeting the protein kinase B (Akt) or Heme oxygenase-1 (HO-1) were administered to investigate their potential protective mechanisms.<BR><B>RESULTS: </B>Our results demonstrated that in animal experiments, Emodin mitigated barrier disruption, minimized inflammation, reduced oxidative stress, and inhibited apoptosis. When Akt or HO-1 was inhibited, the protective effect of Emodin was eliminated. Inhibiting Akt also reduced the level of HO-1. In cell experiments, Emodin reduced inflammation and apoptosis in the OGD/R cell model. Additionally, when Akt or HO-1 was inhibited, the protective effect of Emodin was weakened.<BR><B>CONCLUSIONS: </B>Our findings suggest that Emodin may protect the intestine against II/R injury through the Akt/HO-1 signaling pathway.